Skin Fungi from Colonization to Infection

Abstract

Humans are exceptional among vertebrates in that their living tissue is directly exposed to the outside world. In the absence of protective scales, feathers, or fur, the skin has to be highly effective in defending the organism against the gamut of opportunistic fungi surrounding us. Most (sub)cutaneous infections enter the body by implantation through the skin barrier. On intact skin, two types of fungal expansion are noted: (A) colonization by commensals, i.e., growth enabled by conditions prevailing on the skin surface without degradation of tissue, and (B) infection by superficial pathogens that assimilate epidermal keratin and interact with the cellular immune system. In a response-damage framework, all fungi are potentially able to cause disease, as a balance between their natural predilection and the immune status of the host. For this reason, we will not attribute a fixed ecological term to each species, but rather describe them as growing in a commensal state (A) or in a pathogenic state (B).

FIGURE 1

Overview of basic types of fungal occurrence on human skin and modes of transmission.

FIGURE 2

Maximum likelihood phylogenetic tree (RAxML v.8.0.0) based on ITS and partial LSU, TUB, and 60S L10 sequences of Arthrodermataceae species using GTRCAT as model, with 1,000 bootstrap replications, shown as collapsed when bootstrap values >70%. Guarromyces ceretanicus was selected as outgroup. Reprinted from de Hoog et al. (13).

FIGURE 3

Malassezia species tree was constructed using concatenated sequences of 164 core eukaryotic genes that are present in all Malassezia, U. maydis, and S. cerevisiae genomes. Sequences were aligned using MUSCLE and the phylogeny constructed using a maximum likelihood (ML) approach by RAxML. RAxML was run using “–f a –m PROTGAMMAJTT” with 400 bootstraps.

FIGURE 4

Synthesis of indole-derived pigments by one enzymatic step (TAM1) and possible intervention by TAM inhibitors.